The goal of this protocol is to use a targeted serotonergic manipulation (tryptophan depletion: ATD) and specific neurocognitive and neuroimaging paradigms to consider the role of serotonin in emotional processing. Our goal was to evaluate claims that serotonin has a role in the effective processing of aversive signals. In addition, we will examine whether tryptophan depletion will attenuate the neural response to aversive material. More recently we have been examining interactions between the impact of tryptophan depletion and whether individuals are carriers of the short form of the serotoning transporter gene or are long form homozygotes for this gene. We have found that tryptophan can have a differential effect on individuals who are short form carriers and long form homozygotes and that this appears to be task specific. For emotional learning tasks involving the processing of punishment information, ATD particularly disrupts the ability of individuals who are long form homozygotes. In contrast, for tasks of affective social cognition, such as fearful expression recognition, ATD particularly disrupts the performance of individuals who are s carriers. The implications of these results are being explored in current work.